The very young magnesium (Mg)-deficient mammal may experience a sudden, acute, self-limited shock-like syndrome characterized by apnea; bradycardia, with cardiac arrhythmia; pallor or cyanosis; neuromuscular hyperirritability; and sometimes respiratory distress; resulting in spontaneous recovery or sudden death. Studies in weanling rats have identified stresses that may provoke this state; biochemical changes during the acute episode (increased plasma osmolality, metabolic acidosis, increased plasma Mg, LDH, CPK, SGOT, SGPT, etc.); and post-mortem changes which are chiefly intrathoracic (pulmonary edema, hemmorhage, atelectasis, with overexpansion). A retrospective analysis of data from 249 human infants hospitalized with idiopathic apnea has identified two somewhat similar syndromes: 1) in the neonatal period, and 2) in the post-neonatal period, with a peak incidence at 2 or 3 months of age. Seventy-four percent of all infants tested showed plasma Mg levels at or below the Hospital's lower limit of normal, 1.6 mEq per liter, despite concomitant biochemical events that would increase these levels, including acidosis, hypoxemia, and hemo-concentration. Parenteral Mg load testing usually showed high retention of Mg. One-third of the 249 infants received a minimum of 5 days of Mg therapy, while two-thirds did not. The premature infants constituted the largest subgroup of patients, and only their data achieved statistical significance. Among the premature infants, 61 were Mg-treated, receiving 11.4 days of Mg therapy, while 140 received 0.54 days of therapy. During an 18-month follow-up period, none of 60 treated infants followed were readmitted for apnea, while 29 of 134 untreated infants followed were readmitted for apnea (P less than 0.0005) 31 times. The Mg-treated infants survived; 6 of the 140 untreated infants died (N.S.), two during the first admission. Future studies will focus on a controlled prospective clinical trial of Mg in human infants and on further anatomical and biochemical studies in the animal model.